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Biomedical subjects

V R Pickles

Publications and source records attributed to V R Pickles.

At least 19 recordsLinked to original sources

Neurosteroids and aggressive behaviour in Alzheimer's disease.

Aggressive behaviour is often the most troublesome aspect of Alzheimer's disease. The precise cause is unknown, and there is no fully effective and safe pharmacotherapy. I postulate that (in addition to other possible factors) there is an imbalance between those neurosteroids that facilitate cortical activity and those that restrain it, either through GABAergic neurons or other intermediates or directly on cortical glutamatergic neurons. It is suggested that this hypothesis may be tested experimentally. Positive results could lead to advances in treatment.

Aggression↗

Medical womanpower.

Explore the source record for details and available documents.

Education, Medical, Undergraduate↗

Prostaglandins and dysmenorrhea. Historical survey.

This survey traces the development of the main ideas and experimental findings on the function of endometrial prostaglandins in stimulating the expulsive contractions of the myometrium during normal menstruation, and the effect of excessive action of this nature in producing dysmenorrhea. Some observations are also given on the 'menotoxin', an unidentified substance which is toxic to certain plants and which may or may not prove relevant to gynecology. Areas where further fundamental work is needed are suggested. The survey is not a complete review of the topic, which would need a much longer paper.

Dysmenorrhea↗

Spasmogenic and potentiating actions of some amino acids on the guinea-pig myometrium.

1 Thirty-three amino acids were applied separately in concentrations of 2 to 10 mM to guinea-pig uterine horns in vitro at pH 7.4. About half the acids regularly produced contractions.2 Glycine and the straight-chain L-alpha-amino acids up to norleucine were active (longer ones not tested); D-isomers were less potent or inactive in these concentrations. The omega-amino acids gamma-aminobutyric acid (GABA) and delta-aminovaleric, and the alpha,omega-diamino acids L-alpha,beta-diaminopropionic and L-alpha,gamma-diaminobutyric were active, whereas others of similar chain-length such as beta-alanine and lysine were not. The diacidic acids, glutamic and homocysteic, were more active than the amido-amino acids, glutamine and asparagine. Histidine and phenylalanine showed little or no activity.3 The use of appropriate blocking agents indicated that the responses to representative acids were not mediated by histamine, 5-hydroxytryptamine, acetylcholine, noradrenaline or by prostaglandins. Attempts to block the actions of glycine and GABA with strychnine, thebaine, picrotoxin, bicuculline or tetramethylenedisulphotetramine (TETS) were unsuccessful.4 When some of the acids that were spasmogenic at 2 to 10 mM were applied at sub-spasmogenic doses, they transiently potentiated other spasmogens such as oxytocin or acetylcholine. This effect was also shown by a mixture of amino acids at approximately the normal plasma concentrations.5 There is some similarity between the spasmogenic activities of different amino acids and their known abilities to depolarize neurones.

Acetylcholine↗

Interaction of prostaglandin E 1 and calcium in the guinea-pig myometrium.

1. Prostaglandin E(1) (PGE(1)) increased the responses of guinea-pig myometrium in a low calcium medium to added Ca(2+), acetylcholine, vasopressin, Ba(2+) and Sr(2+). The concentration of PGE(1) used (50 pg/ml) was clearly below the threshold for direct spasmogenesis. In the presence of PGE(1) the doses necessary for half-maximal contractions were decreased by factors of 2.6 for Ca(2+), 2.4 for acetylcholine, and 3.7 for vasopressin. The responses to Ba(2+) or Sr(2+), though studied less extensively, were found to be affected in much the same manner.2. The K(+) depolarized myometrium in a low Ca(2+) medium contracts in response to added Ca(2+). These responses also were increased by low concentrations of PGE(1), but the effective concentration of PGE(1) was indistinguishable from that for direct spasmogenesis.3. Possible mechanisms for the interaction of PGE(1) and Ca(2+) in the myometrium are discussed. It is tentatively suggested that these findings may be relevant to the physiological control of human myometrium.

Acetylcholine↗